<scp>UCA</scp>1 promotes cell proliferation and invasion of gastric cancer by targeting <scp>CREB</scp>1 sponging to miR‐590‐3p

Gu, Lei; Lü, Lei; Zhou, Donglei; Liu, Zhong-chen

doi:10.1002/cam4.1310

Cited by 50 publications

(33 citation statements)

References 21 publications

(22 reference statements)

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“…SATB1 is a target of miR-495-3p and positively correlated with the advanced tumor node metastasis stage of GC [66]. Furthermore, UCA1 could sponge the miR-590-3p targeting cyclic adenosine monophosphate response element-binding protein 1 (CREB1), and knockdown of CREB1 inhibits the growth of human GC in vitro and in vivo [67,68]. Moreover, UCA1 increased multi-drug resistance of GC by downregulating miR-27b [69].…”

Section: Gastrointestinal Cancersmentioning

confidence: 99%

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Xuan

Zhang

et al. 2019

FEBS Letters

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Long non-coding RNAs (lncRNAs) are a major subset of highly conserved non-coding RNAs (ncRNAs) that consist of at least 200 nucleotides and have limited protein-coding potential. Cumulative data have shown that lncRNAs are deregulated in many types of cancer and may control pathophysiological processes of cancer at various levels, including transcription, post-transcription and translation. Recently, lncRNAs have been demonstrated to interact with microRNAs (miRNAs), another major subset of ncRNAs, which regulate physiological and pathological processes by inhibiting target mRNA translation or promoting mRNA degradation. The lncRNA urothelial carcinomaassociated 1 (UCA1) has recently gained much attention as it is overexpressed in many types of cancer and is involved in carcinogenesis. Here, we review the crosstalk between UCA1 and miRNAs during the pathogenesis of cancer, with a focus on cancer-cell proliferation, invasion, drug resistance, and metabolism.

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Section: Gastrointestinal Cancersmentioning

confidence: 99%

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Xuan

Zhang

et al. 2019

FEBS Letters

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“…*P < 0.05, **P < 0.01 miRGen. Previously, CREB1 has been demonstrated to be involved in the regulation of various malignancies, including GBM [31,32]. Furthermore, it has been shown that several oncogenic miRNAs are activated by CREB1 transcriptionally, resulting in the facilitation of cancer development [30,33].…”

Section: Discussionmentioning

confidence: 99%

“…With the aid of miRGen (http://carol ina.imis.athen a-innov ation .gr/diana _tools /web/index .php?r=mirge nv3%2Find ex), we found that CREB1 was a potent transcription factor for miR-1204. In addition, it has been manifested by previous studies that CREB1 is a transcriptional factor and exerts carcinogenic role in tumors [31,32]. Besides, CREB1 can activate certain oncogenic miRNAs through binding to their promoters [30,33].…”

Section: Mir-1204 Was Transcriptionally Activated By Creb1 In Gbmmentioning

confidence: 98%

“…The proto-oncogenic miR-744 is induced by c-JUN at transcriptional level in non-small cell lung cancer [29]. Additionally, cAMP responsive element binding protein 1 (CREB1), known as a transcription factor participating in the metabolism and DNA repair [30], has been demonstrated to be cancer-promoting in various malignancies, including GBM [31,32]. Further, existing studies of cancers have reported that CREB1 could induce the transactivation of oncogenic miRNAs, such as miR-23a and miR-302a [30,33].…”

Section: Introductionmentioning

confidence: 99%

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CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2

Zhao¹,

Shen²,

Ma³

et al. 2020

Cancer Cell Int

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Background: Glioblastoma (GBM) is a subclass of brain malignancy with unsatisfactory prognosis. MicroRNAs (miR-NAs) are a group of non-coding RNAs (ncRNAs) that exert key function on tumorigenesis and tumor development. Purposes: The purpose of this work was to unravel the biological behavior and mechanism of miR-1204 in GBM. Methods: Expressions of miR-1204, NR3C2 and CREB1 were detected by RT-qPCR and western blot. Proliferation and apoptosis of GBM cells were detected by CCK-8, colony formation, caspase-3 activity and TUNEL assays. Molecular interplays were examined by ChIP, RIP, and luciferase reporter assays. Results: MiR-1204 level was elevated in GBM cell lines. Functionally, miR-1204 aggravated cell proliferation whereas suppressed cell apoptosis in GBM cells. Mechanistically, cAMP Responsive Element Binding Protein 1 (CREB1) bound to the promoter of miR-1204 and activated the transcription of miR-1204. Furthermore, miR-1204 targeted and inhibited Nuclear receptor subfamily 3 group C member 2 (NR3C2), a tumor suppressor gene in GBM cells. Rescue assays indicated that NR3C2 participated in the regulation of miR-1204 on the malignant phenotype of GBM cells. Conclusions: We observed for the first time that CREB1-induced miR-1204 promoted malignant phenotype of GBM through targeting NR3C2, indicating that miR-1204 acted as a novel oncogenic miRNA in GBM.

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“…Our previous study also found that H19 could affect melanogenesis by a paracrine effect (Pei et al, 2018). LncRNA UCA1 was first discovered in bladder cancer (Li et al, 2015;Li et al, 2017b) and is also involved in the development of various tumors, such as breast cancer (Liu et al, 2016;Wu and Luo, 2016), nonesmall cell lung cancer (Wu and Zhou, 2018), gastric cancer (Gu et al, 2018), and liver cancer (Hu et al, 2018;Li et al, 2017c). Studies have demonstrated that UCA1 can regulate downstream target molecules by competitively binding to miRNAs (Li et al, 2018a;Liang et al, 2018).…”

Section: Introductionmentioning

confidence: 90%

The Long Noncoding RNA UCA1 Negatively Regulates Melanogenesis in Melanocytes

Pei

Chen

et al. 2020

Journal of Investigative Dermatology

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The long noncoding RNA UCA1 was first discovered in bladder cancer and is known to regulate the proliferation and migration of melanoma. However, its role in melanogenesis is unclear. In this study, we aimed to explore the role and mechanism of UCA1 in melanogenesis. Our findings showed that the expression of UCA1 was negatively correlated with melanin content in melanocytes and pigmented nevus. Overexpression of UCA1 in melanocytes decreased melanin content and the expression of melanogenesis-related genes, whereas knockdown of UCA1 in melanocytes had the opposite effect. High-throughput sequencing revealed that microphthalmia-associated transcription factor (MITF), an important transcription factor affecting melanogenesis, was also negatively correlated with the expression of UCA1. Furthermore, the transcription factor CRE-binding protein (CREB), which promotes MITF expression, was negatively regulated by UCA1. The cAMP/ protein kinase A (PKA), extracellular signaleregulated kinase (ERK), and c-Jun N-terminal kinase (JNK) signaling pathways, which are upstream of the CREB/MITF/melanogenesis axis, were activated or inhibited in response to silencing or enhancing UCA1 expression, respectively. In addition, enhanced UCA1 expression downregulates the expression of melanogenesis-related genes induced by UVB in melanocytes. In conclusion, UCA1 may negatively regulate the CREB/MITF/melanogenesis axis through inhibiting the cAMP/PKA, ERK, and JNK signaling pathways in melanocytes. UCA1 may be a potential therapeutic target for the treatment of pigmented skin diseases.

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UCA1 promotes cell proliferation and invasion of gastric cancer by targeting CREB1 sponging to miR‐590‐3p

Cited by 50 publications

References 21 publications

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2

The Long Noncoding RNA UCA1 Negatively Regulates Melanogenesis in Melanocytes

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